Casey G, Yamanaka Y, Friess H, Kobrin M S, Lopez M E, Buchler M, Beger H G, Korc M
Department of Cancer Biology, Cleveland Clinic Foundation, OH 44195.
Cancer Lett. 1993 May 14;69(3):151-60. doi: 10.1016/0304-3835(93)90168-9.
Pancreatic expression of the p53 tumor suppressor gene was studied in pancreatic adenocarcinomas and chronic pancreatitis. By immunohistochemistry, 16 of 34 (47%) cancers and none of the 24 chronic pancreatitis samples revealed nuclear staining. Sequence analysis indicated that 8 of 24 (33%) cancers were mutated for the p53 gene. Point substitutions occurred at codons 35, 105, 133, 213, 213, 258, and 299. A three base-pair in-frame insertion was identified between codons 261 and 262. None of 8 chronic pancreatitis samples exhibited p53 gene mutations. These data support a role for p53 gene alterations in human pancreatic cancer, and suggest that loss of its regulatory functions may constitute one of the differences between pancreatic cancer and chronic pancreatitis.
在胰腺腺癌和慢性胰腺炎中研究了p53肿瘤抑制基因的胰腺表达。通过免疫组织化学，34例癌症中有16例（47%）显示核染色，而24例慢性胰腺炎样本均未显示核染色。序列分析表明，24例癌症中有8例（33%）p53基因发生突变。点突变发生在密码子35、105、133、213、213、258和299处。在密码子261和262之间发现了一个三碱基对的框内插入。8例慢性胰腺炎样本均未出现p53基因突变。这些数据支持p53基因改变在人类胰腺癌中的作用，并表明其调节功能的丧失可能是胰腺癌与慢性胰腺炎之间的差异之一。
